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Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture
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| Zeitschriftentitel: | Hypertension |
|---|---|
| Personen und Körperschaften: | , , |
| In: | Hypertension, 37, 2001, 5, S. 1336-1340 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Ovid Technologies (Wolters Kluwer Health)
|
| Schlagwörter: |
| author_facet |
Skurk, Thomas Lee, Yu-Mi Hauner, Hans Skurk, Thomas Lee, Yu-Mi Hauner, Hans |
|---|---|
| author |
Skurk, Thomas Lee, Yu-Mi Hauner, Hans |
| spellingShingle |
Skurk, Thomas Lee, Yu-Mi Hauner, Hans Hypertension Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture Internal Medicine |
| author_sort |
skurk, thomas |
| spelling |
Skurk, Thomas Lee, Yu-Mi Hauner, Hans 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.37.5.1336 <jats:p> <jats:italic>Abstract</jats:italic> —Plasminogen activator inhibitor (PAI)-1 is the main inhibitor of the fibrinolytic system and was recently shown to be produced by adipose cells. Obesity is associated with an increased production and release of PAI-1 protein. The aim of this study was to investigate the role of angiotensin (Ang) II and its degradation products for PAI-1 release from human adipose cells. For this purpose, we used the model of in vitro differentiated human adipocytes in primary culture. Exposure of human adipocytes to Ang II resulted in a dose- and time-dependent stimulation of PAI-1 release into the culture medium. The maximum effect of Ang II was found at a concentration of 10 <jats:sup>−5</jats:sup> mol/L for 48 hours, increasing PAI-1 release by 276±53% compared with control cultures ( <jats:italic>P</jats:italic> <0.05). This stimulation was preceded by an increase in specific PAI-1 mRNA copies by 65±12% ( <jats:italic>P</jats:italic> <0.05), with a maximum after 6 hours. Incubation of adipocytes with 10 <jats:sup>−5</jats:sup> mol/L Ang III and Ang IV, respectively, also resulted in a stimulation of PAI-1 release into the medium by 195±60% ( <jats:italic>P</jats:italic> <0.05) and 142±24% ( <jats:italic>P</jats:italic> <0.05), respectively, compared with control cultures. Addition of the angiotensin-receptor subtype 1 (AT <jats:sub>1</jats:sub> ) blocker candesartan abolished the stimulatory action of Ang II and its metabolites, indicating that this effect is mediated by AT <jats:sub>1</jats:sub> . Addition of the AT <jats:sub>1</jats:sub> blocker alone to unstimulated cultures reduced PAI-1 release by 41%±25% ( <jats:italic>P</jats:italic> <0.05), suggesting that endogenous Ang II synthesis contributes to PAI-1 secretion from adipose tissue in an autocrine/paracrine manner. In conclusion, Ang II and its metabolites promote PAI-1 production and release by human fat cells and may contribute to the impairment of the fibrinolytic system typical for obesity. AT <jats:sub>1</jats:sub> receptor blockade reduces basal and abolishes Ang II–stimulated PAI-1 release from human adipocytes. </jats:p> Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture Hypertension |
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Ovid Technologies (Wolters Kluwer Health), 2001 |
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Ovid Technologies (Wolters Kluwer Health), 2001 |
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2001 |
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Hypertension |
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49 |
| title |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_unstemmed |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_full |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_fullStr |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_full_unstemmed |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_short |
Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_sort |
angiotensin ii and its metabolites stimulate pai-1 protein release from human adipocytes in primary culture |
| topic |
Internal Medicine |
| url |
http://dx.doi.org/10.1161/01.hyp.37.5.1336 |
| publishDate |
2001 |
| physical |
1336-1340 |
| description |
<jats:p>
<jats:italic>Abstract</jats:italic>
—Plasminogen activator inhibitor (PAI)-1 is the main inhibitor of the fibrinolytic system and was recently shown to be produced by adipose cells. Obesity is associated with an increased production and release of PAI-1 protein. The aim of this study was to investigate the role of angiotensin (Ang) II and its degradation products for PAI-1 release from human adipose cells. For this purpose, we used the model of in vitro differentiated human adipocytes in primary culture. Exposure of human adipocytes to Ang II resulted in a dose- and time-dependent stimulation of PAI-1 release into the culture medium. The maximum effect of Ang II was found at a concentration of 10
<jats:sup>−5</jats:sup>
mol/L for 48 hours, increasing PAI-1 release by 276±53% compared with control cultures (
<jats:italic>P</jats:italic>
<0.05). This stimulation was preceded by an increase in specific PAI-1 mRNA copies by 65±12% (
<jats:italic>P</jats:italic>
<0.05), with a maximum after 6 hours. Incubation of adipocytes with 10
<jats:sup>−5</jats:sup>
mol/L Ang III and Ang IV, respectively, also resulted in a stimulation of PAI-1 release into the medium by 195±60% (
<jats:italic>P</jats:italic>
<0.05) and 142±24% (
<jats:italic>P</jats:italic>
<0.05), respectively, compared with control cultures. Addition of the angiotensin-receptor subtype 1 (AT
<jats:sub>1</jats:sub>
) blocker candesartan abolished the stimulatory action of Ang II and its metabolites, indicating that this effect is mediated by AT
<jats:sub>1</jats:sub>
. Addition of the AT
<jats:sub>1</jats:sub>
blocker alone to unstimulated cultures reduced PAI-1 release by 41%±25% (
<jats:italic>P</jats:italic>
<0.05), suggesting that endogenous Ang II synthesis contributes to PAI-1 secretion from adipose tissue in an autocrine/paracrine manner. In conclusion, Ang II and its metabolites promote PAI-1 production and release by human fat cells and may contribute to the impairment of the fibrinolytic system typical for obesity. AT
<jats:sub>1</jats:sub>
receptor blockade reduces basal and abolishes Ang II–stimulated PAI-1 release from human adipocytes.
</jats:p> |
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| description | <jats:p> <jats:italic>Abstract</jats:italic> —Plasminogen activator inhibitor (PAI)-1 is the main inhibitor of the fibrinolytic system and was recently shown to be produced by adipose cells. Obesity is associated with an increased production and release of PAI-1 protein. The aim of this study was to investigate the role of angiotensin (Ang) II and its degradation products for PAI-1 release from human adipose cells. For this purpose, we used the model of in vitro differentiated human adipocytes in primary culture. Exposure of human adipocytes to Ang II resulted in a dose- and time-dependent stimulation of PAI-1 release into the culture medium. The maximum effect of Ang II was found at a concentration of 10 <jats:sup>−5</jats:sup> mol/L for 48 hours, increasing PAI-1 release by 276±53% compared with control cultures ( <jats:italic>P</jats:italic> <0.05). This stimulation was preceded by an increase in specific PAI-1 mRNA copies by 65±12% ( <jats:italic>P</jats:italic> <0.05), with a maximum after 6 hours. Incubation of adipocytes with 10 <jats:sup>−5</jats:sup> mol/L Ang III and Ang IV, respectively, also resulted in a stimulation of PAI-1 release into the medium by 195±60% ( <jats:italic>P</jats:italic> <0.05) and 142±24% ( <jats:italic>P</jats:italic> <0.05), respectively, compared with control cultures. Addition of the angiotensin-receptor subtype 1 (AT <jats:sub>1</jats:sub> ) blocker candesartan abolished the stimulatory action of Ang II and its metabolites, indicating that this effect is mediated by AT <jats:sub>1</jats:sub> . Addition of the AT <jats:sub>1</jats:sub> blocker alone to unstimulated cultures reduced PAI-1 release by 41%±25% ( <jats:italic>P</jats:italic> <0.05), suggesting that endogenous Ang II synthesis contributes to PAI-1 secretion from adipose tissue in an autocrine/paracrine manner. In conclusion, Ang II and its metabolites promote PAI-1 production and release by human fat cells and may contribute to the impairment of the fibrinolytic system typical for obesity. AT <jats:sub>1</jats:sub> receptor blockade reduces basal and abolishes Ang II–stimulated PAI-1 release from human adipocytes. </jats:p> |
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| spelling | Skurk, Thomas Lee, Yu-Mi Hauner, Hans 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.37.5.1336 <jats:p> <jats:italic>Abstract</jats:italic> —Plasminogen activator inhibitor (PAI)-1 is the main inhibitor of the fibrinolytic system and was recently shown to be produced by adipose cells. Obesity is associated with an increased production and release of PAI-1 protein. The aim of this study was to investigate the role of angiotensin (Ang) II and its degradation products for PAI-1 release from human adipose cells. For this purpose, we used the model of in vitro differentiated human adipocytes in primary culture. Exposure of human adipocytes to Ang II resulted in a dose- and time-dependent stimulation of PAI-1 release into the culture medium. The maximum effect of Ang II was found at a concentration of 10 <jats:sup>−5</jats:sup> mol/L for 48 hours, increasing PAI-1 release by 276±53% compared with control cultures ( <jats:italic>P</jats:italic> <0.05). This stimulation was preceded by an increase in specific PAI-1 mRNA copies by 65±12% ( <jats:italic>P</jats:italic> <0.05), with a maximum after 6 hours. Incubation of adipocytes with 10 <jats:sup>−5</jats:sup> mol/L Ang III and Ang IV, respectively, also resulted in a stimulation of PAI-1 release into the medium by 195±60% ( <jats:italic>P</jats:italic> <0.05) and 142±24% ( <jats:italic>P</jats:italic> <0.05), respectively, compared with control cultures. Addition of the angiotensin-receptor subtype 1 (AT <jats:sub>1</jats:sub> ) blocker candesartan abolished the stimulatory action of Ang II and its metabolites, indicating that this effect is mediated by AT <jats:sub>1</jats:sub> . Addition of the AT <jats:sub>1</jats:sub> blocker alone to unstimulated cultures reduced PAI-1 release by 41%±25% ( <jats:italic>P</jats:italic> <0.05), suggesting that endogenous Ang II synthesis contributes to PAI-1 secretion from adipose tissue in an autocrine/paracrine manner. In conclusion, Ang II and its metabolites promote PAI-1 production and release by human fat cells and may contribute to the impairment of the fibrinolytic system typical for obesity. AT <jats:sub>1</jats:sub> receptor blockade reduces basal and abolishes Ang II–stimulated PAI-1 release from human adipocytes. </jats:p> Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture Hypertension |
| spellingShingle | Skurk, Thomas, Lee, Yu-Mi, Hauner, Hans, Hypertension, Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture, Internal Medicine |
| title | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_full | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_fullStr | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_full_unstemmed | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_short | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| title_sort | angiotensin ii and its metabolites stimulate pai-1 protein release from human adipocytes in primary culture |
| title_unstemmed | Angiotensin II and Its Metabolites Stimulate PAI-1 Protein Release From Human Adipocytes in Primary Culture |
| topic | Internal Medicine |
| url | http://dx.doi.org/10.1161/01.hyp.37.5.1336 |